Chapter 8 Cardiac Pathology Flashcards
1
Q
What is the most common cause of Ischemic Heart Disease and what are the risk factors?
A
Atherosclerosis. Risk factors are similar to those of atherosclerosis; incidence increases with age
2
Q
What is stable angina?
A
chest pain that arises with exertion or emotional distress, does not occur at rest
3
Q
What is stable angina due to?
A
atherosclerosis of coronary arteries with >70% stenosis; decreased blood flow is not able to meet the metabolic demands of the myocardium during exertion
4
Q
What does stable angina represent?
A
reversible injury to myocytes ( no necrosis)
5
Q
What is a hallmark sign of reversible cell damage?
A
cell swelling
6
Q
How does stable angina present?
A
chest pain (lasting <20 min) that radiates to the left arm or jaw, diaphoresis, and shortness of breath.
7
Q
What does EKG show with stable angina?
A
ST-segment depression due to subendocardial ischemia
8
Q
What relieves stable angina?
A
Rest or nitroglycerin (decreases preload)
9
Q
What is unstable angina?
A
chest pain that occurs at rest (still reversible)
10
Q
What is unstable angina usually due to?
A
rupture of an atherosclerotic plaque with thrombosis and INCOMPLETE occlusion of a coronary artery
11
Q
What type of injury does unstable angina represent?
A
reversible
12
Q
What does EKG show in unstable angina?
A
ST-depression
13
Q
What relieves unstable angina?
A
nitro
14
Q
What does unstable angina carry a high risk for?
A
progression to MI
15
Q
What is Prinzmetal angina?
A
episodic chest pain unrelated to exertion
16
Q
What is prinzmetal angina due to?
A
vasospasm of coronary artery (completely shuts it)
17
Q
What type of injury does prinzmetal angina represent?
A
reversible
18
Q
What does EKG show in prinzmetal angina?
A
ST segement elevation due to transmural ischemia
19
Q
What relieves prinzmetal angina?
A
Nitro or Ca channel blockers.
20
Q
What type of cell injury occurs in MI?
A
necrosis of myocytes which is irreversible
21
Q
What is usually the cause of MI?
A
rupture of an atherosclerotic plaque with thrombosis and COMPLETE occlusion of a coronary artery
22
Q
What are some other causes of MI? (3)
A
coronary artery vasospasm (due to prinzmetal angina or cocaine use)
Emboli
Vasculitis (Kawasaki disease)
23
Q
What are the clinical features of an MI?
A
severe crushing chest pain (lasting >20 min) that radiates to left arm or jaw, diaphoresis, and dyspnea (due to pulmonary congestion)
24
Q
How are each of the four chambers of the heart usually affected in an MI?
A
Infarction usually incolves the LV: RV,RA,LA are generally spared.
25
What does occlusion of the LAD lead to in MI?
infarction of the anterior wall and anterior septum of the LV; LAD is most commonly involved artery in MI
26
What does occlusion of the RCA cause in MI?
leads to infarction of the posterior wall, posterior septum, and papillary muscles of the LV: RCA is the second most commonly involved artery in MI
27
What does occlusion of the left circumflex artery cause in MI?
infarction of the lateral wall of the LV
28
What portions of the wall are damaged initially in MI and what does EKG show?
Initially subendocardial necrosis involving less than 50% of the wall leads to ST-depression
29
What portions of the wall become damages with continued ischemia in an MI and what EKG changes are seen?
transmural necrosis involving most of the myocardial wall causing ST-elevation on EKG
30
What two cardiac enzymes become elevated in MI?
Troponin I and CK-MB
31
Describe the time course and level of troponin I after an MI?
Troponin I is the most sensitive and specific marker for MI. levels rise 2-4 hours after infarction, peak at 24 hours, and return to normal by 7-10 days
32
describe the time course and level of CK-MB after an MI?
CK-MB is used for detecting reinfarction that occurs days after an initial MI. levels rise in 4-6 hours, peak at 24, and return to normal by 72.
33
Name 6 pharmacological treatments of MI
1 ASA and/or Heparin - limits thrombosis
2 Supplemental oxygen - minimizes ischemia
3 Nitrates - vasodilate veins and coronary arteries
4 BB slows HR, decreasing oxy demand and risk for arrhythmia
5 ACE-I decreases LV dilation
6 Fibrinolysis or angioplasty- opens blocked vessel
34
What does reperfusion of ireversibly damaged cells cause?
can result in calcium influx, leading to hypercontraction of myofibrils (Contraction band necrosis)
35
Describe reperfusion injury and how this would show up in labs?
Return of oxygen and inflammatory cells may lead to free radical generation further damaging myocytes. Cardiac enzymes would continue to rise even after opening blocked vessels.
36
What are the gross and microscopic changes and complications from 0-4 hours following an MI?
Gross- NONE
Microscopic - NONE
Complications- Cardiogenic shock (massive infarction), CHF, arrythmia
37
What are the gross and microscopic changes and complications from 4-24 hours following an MI?
Gross- Dark discoloration
microscopic - coagulative necrosis
complications- arrhythmia (if it doesnt happen by now it probably wont happen)
38
What are the gross and microscopic changes and complications from 1-3 days following an MI?
Gross- yellow pallor
microscopic- neutrophils
complications - fibrinous pericarditis (only with transmural injury); presents as chest pain with friction rub
39
What are the gross and microscopic changes and complications from 4-7 days following an MI?
Gross - yellow pallor
microscopic - macrophages
complications - this is the time when the wall is the weakest. rupture of ventricular free wall (leads to cardiac tamponade), interventricular septum (leads to shunt), or papillary muscle (leads to mitral insufficiency)
40
What are the gross and microscopic changes and complications from 1-3 weeks following an MI?
Gross - red border emerges as granulation tissue enters from edge of infarct.
microscopic - granulation tissue with plump fibroblasts, collagen, and BV
complications - none in chart
41
What are the gross and microscopic changes and complications in the months following an MI?
gross - white scar (weaker than healthy tissue)
microscopic - fibrosis
complications - aneurysm, mural thrombus, or Dressler syndrome
42
What is Dressler syndrome?
autoimmune pericarditis due to antigen exposure after an MI usually 6-8 weeks post infarct.
43
What is Sudden cardiac death? what usually causes it?
Unexpected death due to cardiac disease: occurs without symptoms or <1 hours after symptoms arise. usually due to fatal ventricular arrhythmia
44
What is the most common etiology of sudden cardiac death?
acute ischemia; 90% of patients have preexisting severe atherosclerosis.
45
What are some less common causes of sudden cardiac death?
mitral valve prolapse, cardiomyopathy, and cocaine abuse (vasospasm)
46
What is chronic ischemic heart disease? What does it progress to?
Poor myocardial function due to chronic ischemic damages (with or without infarction); progresses to CHF
47
What are 5 causes of left-sided heart failure?
1 ischemia
2 hypertension leads to concentric hypertrophy, thicker wall, more difficult to fill
3 dilated cardiomyopathy
4 MI
5 restrictive cardiomyopathy (cant fill heart appropriately)
48
What are clinical features of left sided heart failure due to?
decreased forward perfusion and pulmonary congestion.
49
What does pulmonary congestion lead to in left sided heart failure?
leads to pulmonary edema.
results in dyspnea, paroxysmal nocturnal dyspnea, orthopnea, and crackles. Small congested arteries may burst, leading to intraaleolar hemorrhage; marked by hemosiderin-laden macrophages (heart failure cells)
50
What is the consequence of decreased forward perfusion in left sided heart failure?
decreased flow to kidneys leads to activation of RAS system. Fluid retention exacerbates CHF
51
What is the mainstay of treatment for left sided heart failure?
ACE-I
52
What is the most common cause of right sided heart failure and what are two other causes?
most common is left sided heart failure. other important causes include left-to-right shunt and chronic lung disease (cor pulmonale) - develop hypoxia, vessels constrict, pulmonary pressure and resistance increase
53
What are clinical features of right sided heart failure due to?
congestion
54
What are the clinical features of right sided heart failure?
JVD
painful hepatospenlomegaly with characteristic 'nutmeg' liver; may lead to cardiac cirrhosis
dependent pitting edema due to increased hydrostatic pressure.
55
When do congenital heart defects arise and what percent of live births are they seen in? are they mainly sporadic or inherited?
Arise during embryogenesis (usually weeks 3-8); seen in 1% of live births, most are sporadic
56
What do congenital cardiac defects often result in?
Shunting between the left (systemic) and right (pulmonary) circulations
57
Describe how the reversal of a left to right shunt occurs?
increased flow through th epulmonary circulation results in hypertrophy of pulmonary vessels and pulmonary hypertension. Increased pulmonary resistance eventually results in reversal of shunt, leading to late cyanosis (Eisenmenger syndrome) with right ventricular hypertrophy, polycythemia and clubbing.
58
How do defects with right to left shunting present?
usually as cyanosis shortly after birth
59
What is a ventricular septal defect and what is it associated with?
Defect in the septum that divides the right and left ventricles. Most common congenital heart defect. associated with fetal alcohol syndrome.
60
What does a VSD result in? comment of the effects of the size of the defect.
a left to right shunt. The size of the defect determines the extent of the shunting and age at presentation. Small defects are often asymptomatic; large defects can lead to eisenmenger syndrome.
61
What does treatment of a VSD involve?
surgical closure; small defects may close spontaneously.
62
What is an atrial septal defect? what is the most common type?
defect in the septum that divides the right and left atria; most common type is ostium secundum (90%)
63
What is ostium primum associated with?
Down Syndrome
64
What does ASD result in? How can it be detected on examination.
left to right shunt and split S2 on auscultation (Increased blood in right heart delays closure of the pulmonary valve
65
What is an important complication of ASD?
paradoxical emboli - crosses to left heart and lodges in systemic circulation.
66
What is a patent ductus arteriosus and what is it associated with?
failure of ductus arteriosus to close; associated with congenital rubella.
67
Where is the a PDA wrt the major branches of the aorta?
below the major branches
68
What does PDA result in?
left to right shunt between the aorta and the pulmonary artery.
69
Describe the symptoms and signs of a PDA?
Asymptomatic at birth with continuous 'machine-like' murmur; may lead to eisenmenger syndrome, resulting in lower extremity cyanosis.
70
What does treatment of a PDA involve?
indomethacin, which decreases PGE, resulting in PDA closure
71
What is the tetrology of fallot?
1 stenosis of the right ventricular outflow tract
2 right ventricular hypertrophy
3 VSD
4 an aorta that overrides the VSD
72
What does tetrology of fallot lead to?
right to left shunt leads to early cyanosis; degree of stenosis determines the extent of shunting and cyanosis
73
What are some methods patients learn to respond to a cyanotic spell with tetrology of fallot?
learn to squat which increases arterial resistance and decreases shunting and allows more blood to reach lungs
74
What can be seen on X-ray in tetrology of fallot?
'boot-shaped' heart
75
What is transposition of the great arteries?
Characterized by pulmonary artery arising from the left ventricle and aorta arising from the right ventricle.
76
What is transposition of the great arteries associated with?
maternal diabetes
77
What does transposition of the great arteries present with?
early cyanosis; pulmonary and systemic circuits do not mix.
78
What does treatment of transposition of the great arteries entail?
Creation of a shunt after birth is required for survival.
| PGE can be administered to maintain a PDA until definitive surgical repair is performed.
79
What cardiac changes does transposition of the great arteries result in?
hypertrophy of the right ventricle and atrophy of the left ventricle
80
What is truncus arteriosus?
Characterized by a single large vessel arising from both ventricles. truncus fails to divide
81
How does truncus arteriosus present?
presents with early cyanosis; deoxygenated blood from right ventricle mixes with oxygenated blood from left ventricle before pulmonary and aortic circulations separate
82
What is tricuspid atresia? what is seen in the RV?
tricuspid valve oriface fails to develop; right ventricle is hypoplastic
83
What is tricuspid atresia often associated with, what does it result in, and how does it present?
often associated with ASD, resulting in a right to left shunt; presents with early cyanosis
84
What is coarctation of the aorta? what two forms is it generally split into?
narrowing of the aorta; classically divided into infantile and adult forms
85
What is infantile coarctation of the aorta associated (congenital defect) with and where does it usually occur?
Associated with a PDA, lies after the aortic arch but before the PDA
86
How does infantile coarctation of the aorta present and what is it associated with (inherited disease)?
Presents as lower extremity cyanosis in infants, often at birth. is associated with Turner syndrome
87
Is adult coarctation of the aorta associated with a PDA and where does it lie? What other deformity is it associated with?
is NOT associated with a PDA and lies distal to aortic arch. associated with a bicuspid aortic valve
88
How does adult coarctation of the aorta present?
presents as HTN in the upper extremities and hypotension with weak pulses in the lower extremities; classically discovered in adulthood
89
What signs can be seen on xray in aortic coarctation and what is this due to?
collateral circulation develops across the intercostal arteries; engorged arteries cause 'notching' of ribs on x-ray.
90
What do valvular lesions generally result in?
stenosis or regurgitation
91
What is acute rheumatic fever a complication of? who does it usually affect?
systemic complication of pharyngitis due to group A beta hemolytic streptococci; affects children 2-3 weeks after an episode of streptococcal pharyngitis
92
What is Acute rheumatic fever caused by molecularly?
caused by molecular mimicry ; bacterial M protein resembles human tissue
93
How is diagnosis made of acute rheumatic fever?
based on the jones criteria.
1 evidence of prior group A strep infection (elevated ASO or anti-DNase B titers)
2 minor criteria are nonspecific and include fever and elevated ESR
3 Major criteria
94
What are the major criteria for acute rheumatic fever?
```
Migratory polyarthritis
pancarditis
subcutaneous nodules
erythema miarginatum
sydenham chorea
```
95
What is migratory polyarthritis?
swelling and pain in a large joint that resolves within days and "migrates to involve another large joint.
96
Describe the endocarditis in pancarditis of acute rheumatic fever?
mitral valve is involved more commonly than aortic valve. characterized by small vegetations along the lines of closure that lead to regurgitation
97
describe the myocarditis in pancarditits of acute rheumatic fever?
myocarditis with aschoff bodies that are characterized by foci of chronic inflammation, reactive histiocytes with slender, wavy nuclei (Anitschkow cells), giant cells, and fibrinoid material; myocarditis is the most common cause of death during the acute phase
98
What does pericarditis in acute rheumatic fever lead to?
leads to friction rub and chest pain
99
What is erythema marginatum?
annular, nonpruritic rash with erythematous borders, commonly involving the trunk and limbs
100
What is sydenham chorea?
rapid, involuntary muscle movements
101
What is usually the result of an acute attack of rheumatic fever?
Acute attack usually resolves but may progress to chronic rheumatic heart disease; repeat exposure to group A strep results in relapse of the acute phase and increases risk for chronic disease.
102
What is chronic rheumatic heart disease characterized by?
valve scaring that arises as a consequence of rheumatic fever
103
What does chronic rheumatic heart disease result in? what valves are affected?
stenosis with a classic 'fish mouth' appearance.
almost always involves the mitral valve; leads to thickening of chordae tendinae and cusps. occasionally involves the aortic valve; leads to fusion of the commissures. other valves are less frequently involved
104
What do complications of chronic rheumatic heart disease include?
infectious endocarditis
105
What is aortic stenosis?
Narrowing of the aortic valve orifice
106
What is aortic stenosis usually due to?
fibrosis and calcification from 'wear and tear'
107
When does aortic stenosis generally present and what increases the risk for it?
presents in late adulthood (>60 years). bicuspid aortic valve increases risk and hastens disease onset. A normal aortic valve has three cusps; fewer cusps results in increased 'wear and tear' on each remaining cusp
108
What is an alternative way aortic stenosis can arises instead of 'wear and tear' how do you tell the two apart?
may also arise from chronic rheumatic valve disease; coexisting mitral stenosis and fusion of the aortic valve commissures distinguish rheumatic disease from 'wear and tear'
109
what does aortic stenosis lead to? How can it be detected on exam?
cardiac compensation leads to prolonged asymptomatic stage during which a systolic ejection click followed by a crescendo-decrescendo murmur is heard.
110
What do complications of aortic stenosis include? 3
1 concentric left ventricular hypertrophy - may progress to cardiac failure
2 angina and syncope with exercise - limited ability to increase blood flow across the stenotic valve leads to decreased perfusion of the myocardium and brain.
3 microangiopathic hemolytic anemia
111
What is the treatment of aortic stenosis and when is it done?
Treatment is valve replacement AFTER onset of complications
112
What is Aortic Regurgitation?
backflow of blood from the aorta into th eleft ventricle during systole.
113
What does aortic regurgitation arise due to?
aortic root dilation (eg. syphilitic aneurysm and aortic dissection) or valve damage (eg. infectious endocarditis); most common cause is isolated root dilation
114
What are 3 clinical symptoms of aortic regurgitation?
1 early, blowing diastolic murmur
2 Hyperdynamic circulation due to increased pulse pressure
3 LV dilation and eccentric hypertrophy (due to volume overload)
115
Describe the hyperdynamic circulation due to increased pulse pressure in aortic regurgitation?
diastolic pressure decreases due to regurgitation, while systolic pressure increases due to increased stroke volume. presents with bounding pulse (water-hammer pulse), pulsating nail bed (quincke pulse), and head bobbing
116
What is mitral valve prolapse?
Ballooning of mitral valve into left atrium during systole
117
What is mitral valve prolapse due to?
myxoid degeneration (accumulation of ground substance) of the valve, making it floppy
118
What is the etiology of mitral valve prolapse and what syndromes is it associated with?
etiology is unknown; may be seen in marfan or ehlers danlos syndrome
119
How does mitral valve prolapse present?
With an incidental mid-systolic click followed by a regurgitation murmur; usually asymptomatic
120
What can cause the click and murmur of mitral valve prolapse to become softer?
Squatting increases systemic resistance and decreases left ventricular emptying.
121
What complications are seen in mitral valve regurgitation?
complications are rare, but include infectious endocarditis, arrhythmias, and severe mitral regurgitation.
122
What is treatment for mitral valve prolapse?
valve replacement
123
What is mitral valve regurgitation?
reflux of blood from the left ventricle into the left atrium during systole
124
What does mitral valve regurgitation arise as a complication of? 1 main and 4 others
usually mitral valve prolapse; other causes include LV dilatation (left sided heart failure) infective endocarditis, acute rheumatic heart disease, and papillary muscle rupture after a MI
125
What are the clinical feature of mitral valve regurgitation?
holosystolic "blowing" murmur; louder with squatting (increased systemic resistance decreases LV emptying) and expiration (increases return to left atrium) results in volume overload and left sided heart failure.
126
What is mitral stenosis, what is it usually due to?
narrowing of the mitral valve orifice usually due to chronic rheumatic valve disease
127
What are the clinical feature of mitral stenosis?
1 Opening snap followed by a diastolic rumble
| 2 Volume overload leads to dilatation of the left atrium
128
What does dilatation of the left atrium in mitral stenosis lead to?
1 pulmonary congestion with edema and alveolar hemorrhage
2 pulmonary hypertension and eventual right sided heart failure
3 atrial fibrillation with associated risk for mural thrombi
129
What is endocarditis? What is it usually due to?
inflammation of the endocardium that lines the surface of cardiac valves; usually due to bacterial infection
130
What is the most common overall cause of endocarditits, describe its virulence?
Streptoccocus Viridans, low virulence
131
What is required for a strep viridans endocarditis, describe the vegetations?
Infects only previously damaged valves (eg chronic rheumatic heart disease and mitral valve prolapse). results in small vegetations that do not destroy the valve (SUBACUTE ENDOCARDITIS)
132
Describe the pathophysiology of subacute endocarditis with strep viridans?
damaged endocardieal surface develops thrombotic vegetations (platelets and fibrin). Transient bacteremia leads to trapping of bacteria in the vegetations; prophylactic antibiotics decrease risk of endocarditis (dental exams)
133
What is the most common cause of endocarditis in IV drug users, what valve is involved, and what does it result in?
Staph Aureus, high virulence organism that infects normal valves, most commonly the tricuspid. results in large vegetations that destroy the valve (ACUTE ENDOCARDITIS)
134
What organism is associated with the endocarditis of prosthetic valves?
Staph epidermidis
135
What organism is associated with endocarditis of patients with underlying colorectal carcinoma?
Strep Bovis
136
What are the HACEK organisms and what is unique about the endocarditis they cause?
Haemopholus, Actinobacillus, Cardiobacterium, Eikenella, Klingella all are associated with endocarditis with negative blood cultures.
137
What do clinical features of endocarditis include? 4
1 Fever - due to bacteremia
2 murmur - due to vegetations on heart valve
3 Janeway lesions (erythematous nontender lesions on palms and soles), Osler nodes (tender lesions on fingers and toes), splinter hemorrhages in nail bed, and roth spots in retina, all due to embolization of splinter hemmhorages
4 anemia of chronic disease
138
What are the laboratory findings in endocarditis? 3
1 positive blood cultures
2 anemia of chronic disease (decreased Hb, decreased MCV, increased ferritin, decreased TIBC, decreased serum iron, decreased saturation
3 tranesophageal echocardiogram is useful for detecting lesions on valves
139
Describe nonbacterial endocarditis
Sterile vegetations that arise in associated with a hypercoaguable state or underlying adenocarcinoma. Vegetations arise on the mitral valve along lines of closure and result in mitral regurgitation
140
Describe libmann Sacks endocarditis
is due to steril vegetations that arise in association with SLE. Vegetations are present on the surface and undersurface of the mitral valve and result in mitral regurgitation.
141
What is dilated cardiomyopathy?
Dilation of all four chambers of the heart; most common form of cardiomyopathy
142
What does dilated cardiomyopathy result in?
Results in systolic dysfunction (ventricles cannot pump), leading to biventricular CHF; complications include mitral and tricuspid regurgitation and arrhythmia with sudden death, or heart failure. Dilated cardiomyopathy is a late complication.
143
What is the most common cause of dilated cardiomyopathy?
idiopathic
144
What are 6 other causes of dilated cardiomyopathy
1 Genetic mutation (usually autosomal dominant)
2 Myocarditis
3 Alcohol abuse
4 Drugs (Doxorubicin and cocaine)
5 Pregnancy - seen during late pregnancy or soon (weeks to months) after birth
6 Hemochromatosis
145
What is the most common infectious agent causing myocarditis and a dilated cardiomyopathy and what is it characterized by? What are the symptoms
usually due to coxsackie A or B - characterized by a lymphocytic infiltrate in the myocardium; results in chest pain, arrhythmia with sudden death, or heart failure. Dilated cardiomyopathy is a late complication.
146
What is the treatment for a dilated cardiomyopathy?
Heart Transplant
147
What is hypertrophic cardiomyopathy?
massive hypertrophy of the left ventricle
148
What is hypertrophic cardiomyopathy due to?
genetic mutations in sarcomere proteins; most common form is autosomal dominant
149
What are the clinical features of hypertrophic cardiomyopathy? (3)
1 decreased CO- LV hypertrophy eads to diastolic dysfunction (ventricle cannot fill, loss of compliance)
2 Sudden death due to ventricular arrhythmias; hypertrophic cardiomyopathy is a common cause of sudden death in young athletes.
3 syncope with exercise - subaortic hypertrophy of the ventricular septum results in functional aortic stenosis.
150
What does biopsy show in hypertrophic cardiomyopathy?
Shows myofiber hypertrophy with disarray
151
What is restrictive cardiomyopathy?
Decreased compliance of the ventricular endomyocardium that restricts filling during diastole
152
Name five causes of restrictive cardiomyopathy?
```
1 amyloidosis
2 sarcoidosis
3 endocardial fibroelastosis (Children)
4 Loeffler syndrome (endomyocardial fibrosis with an eosinophilic infiltrate with eosinophilia)
5 Hemochromatosis
```
153
How does restrictive cardiomyopathy present?
CHF; classic finding is low-voltage EKG with diminished QRS amplitude
154
What is myxoma?
Benign mesenchymal tumor with a gelatinous appearance and abundant ground substance on histology (most common primary cardiac tumor in adults)
155
What is the appearance and symptoms of a myxoma?
Usually forms a pedunculated mass in the left atrium that causes syncope due to obstruction of the mitral valve
156
What is a rhabdomyoma? Who is it most common in, and what is it associated with?
A benign hamartoma of cardiac muscle (most common primary cardiac tumor in children; associated with tuberous sclerosis)
157
What is more common in the heart; metastatic tumors or primary tumors?
metastatic
158
What are common metastases to the heart?
breast, lung carcinoma, melanoma, lymphoma
159
What do mets to the heart most commonly involve, and what results?
the pericardium; resulting in a pericardial effusion.
